BackgroundRecent studies have found gut microbiota to be closely associated with onset and perpetuation of UC. Currently, studies about gut microbiota have mainly covered samples collected from the intestinal lumen. However, the luminal flora is only part of the gut microbiota. Studies of the changes in mucosal flora under pathological conditions have been lacking. In this study, we investigated the correlation between the onset of UC and flora changes in different intestinal layers.MethodsThe dextran sulfate sodium(DSS)-induced UC model was established by exposing mice to cycles of DSS. The luminal contents, an inner mucus layer, and outer mucus layer were harvested under sterile conditions. The samples were then analyzed using high-throughput sequencing of 16S rRNA V3 + V4 amplicons. The colonic microbiota composition and diversity were analyzed and compared using MetaStat, LefSe, multivariate analysis of variance, and spatial statistics.ResultsThe DSS-induced UC mouse model was successfully established. The diversity of the microbiota from luminal content, the outer mucus layer, and inner mucus layer were significantly different in both control and UC model groups. The statistically different OTUs belonged to Lachnospiraceae and Ruminococcaceae families within the order Clostridiales were mainly localized to the outer mucus layer.ConclusionsThe alterations in flora composition and diversity mainly occurred in the colonic outer mucus layer. The change of flora in the colonic mucus layers is of great significance in the understanding of common features of gut flora in IBD and the understanding of the relationship between gut flora and disease progression.Electronic supplementary materialThe online version of this article (10.1186/s12876-019-0930-3) contains supplementary material, which is available to authorized users.

Intestinal microecology is the main component of human microecology. Intestinal microecology consists of intestinal microbiota, intestinal epithelial cells, and intestinal mucosal immune system. These components are interdependent and establish a complex interaction network that restricts each other. According to the impact on the human body, there are three categories of symbiotic bacteria, opportunistic pathogens, and pathogenic bacteria. The intestinal microecology participates in digestion and absorption, and material metabolism, and inhibits the growth of pathogenic microorganisms. It also acts as the body's natural immune barrier, regulates the innate immunity of the intestine, controls the mucosal barrier function, and also participates in the intestinal epithelial cells' physiological activities such as hyperplasia or apoptosis. When the steady-state balance of the intestinal microecology is disturbed, the existing core intestinal microbiota network changes and leads to obesity, diabetes, and many other diseases, especially irritable bowel syndrome, inflammatory bowel disease (IBD), and colorectal malignancy. Intestinal diseases, including tumors, are particularly closely related to intestinal microecology. This article systematically discusses the research progress on the relationship between IBD and intestinal microecology from the pathogenesis, treatment methods of IBD, and the changes in intestinal microbiota.

BackgroundUlcerative colitis (UC) is a modern refractory disease, and its etiology has been difficult to discern. Studies have shown that UC is closely associated with the gut microbiota. Garidisan is composed of wild poppy and Artemisia frigida Willd and is commonly used for the treatment of UC in Inner Mongolia, China. In clinical settings, Garidisan has been found to treat UC effectively, with low recurrence. Previous studies have shown that Garidisan has a good therapeutic effect on mice with UC, but the therapeutic mechanism is still unclear. In this study, we investigated the regulatory effect of Garidisan on dysbiosis of the gut microbiota in a UC mouse model and explored the possible mechanism of the therapeutic effect of Garidisan on UC.MethodsThe UC mouse model was established by the dextran sulfate sodium (DSS) circulating free water drinking method, and the luminal contents were sampled under sterile conditions. High-throughput sequencing of the 16S rRNA gene V3 + V4 region of the luminal contents of the control group, model group, and Garidisan group was conducted, and clustering of operational taxonomic units (OTUs) and species annotation were performed. The differences in species composition and microbial community structure between individual groups of samples were analyzed using MetaStat, LefSe, rank sum test, and Bayesian causal network analysis.ResultsThe UC mouse model was successfully established and the sequencing results were of adequate quality. There were significant differences in the diversity of luminal contents between the control group, model group, and Garidisan group, and the differences between groups were greater than those within any group. The therapeutic effect of Garidisan on UC is attributed to the direct effect on the Lachnospiraceae family of bacteria.ConclusionGaridisan has a good regulatory effect on the gut microbiota, and Lachnospiraceae could be an important direct target of Garidisan for the treatment of UC.

Background and Purpose: Subarachnoid hemorrhage (SAH) has long been classified into two main forms, aneurysmal SAH (aSAH) and non-aneurysmal SAH (naSAH), but the related risk factors for aSAH and naSAH are heterogeneous. Our objective was to determine the risk factors for SAH of known or unknown origin with respect to diagnostic evaluation in a large patient cohort. We sought to determine whether our classification system can further predict middle long-term stroke and death.Methods: We performed a systematic review and meta-analysis to identify risk factors for each SAH subtype. The discovery phase analyzed 11 risk factors from case studies in the literature. Kruskal-Wallis, Cox regression, logistic regression, and Kaplan-Meier analyses were used to compare the two groups.Results: A total of 14,904 (34.53%) male and 22,801 (52.84%) female patients were eligible for this study. At a median follow-up of 45.6 months, the 5-years overall survival was 97.768% (95% CI: 0.259–0.292) for aSAH patients and 87.904% (95% CI: 1.459–1.643) for naSAH patients. The 10-years survival rate was 93.870% (95% CI: 2.075–3.086) and 78.115% (95% CI: 2.810–3.156), respectively. Multi-risk factor subgroups showed significant intergroup differences. We identified eight risk factors (drugs, trauma, neoplastic, vessels lesion, inflammatory lesion, blood disease, aneurysm, peri-mesencephalic hemorrhage) using logistic regression, which were optimally differentiated among the aSAH [aSAH-S (AUC: 1), a-d-SAH (AUC: 0.9998), aSAH-T (AUC: 0.9199), aSAH-N (AUC: 0.9433), aSAH-V (AUC: 1), aSAH-I (AUC: 0.9954), a-bd-SAH (AUC: 0.9955)] and naSAH [na-pmSAH (AUC: 0.9979), na-ni-ivl-SAH (AUC: 1), na-t-SAH (AUC: 0.9997), na-ne-SAH (AUC: 0.9475), na-d-SAH (AUC: 0.7676)] subgroups. These models were applied in a parallel cohort, showing eight risk factors plus survival rates to predict the prognosis of SAH.Conclusions: The classification of risk factors related to aSAH and naSAH is helpful in the diagnosis and prediction of the prognosis of aSAH and naSAH patients. Further validation is needed in future clinical applications.

BackgroundDiagnosing the well-known concomitant Rathke’s cleft cyst (RCC) and differentiating it from other sellar lesions are difficult because RCC is and other sellar lesions are closely related and represent a continuum from simple RCCs to more complex lesions. The purpose of this study is to better understand the adeno- and neurohypophysis adjacent to the par intermedia remnants and their role in the origin of the coexistence of these two distinct tumor neoplasias; to assess the incidence in different age groups; to categorize the pathohistological subtype, which can be incorporated in predictive/prognostic models; and finally, to evaluate the current evidence on collision tumors of the sellar embryonic remnant tract in terms of their biological behavior and pathology.MethodsUtilizing the PubMed database, data were collected from 1920 to 2019. Information about demographics, clinical characteristics, and age was summarized and analyzed by using univariable and multivariable models. The same cell type was observed regardless of whether the tumor was only one type or mixed types, and their histologic patterns were assessed.ResultsThe incidence rates were similar among patients stratified into three age subgroups: 40–49 years (24.57%), 50–59 years (19.54%), and older than 60 years (22.98%). We found that various types of sellar lesions, namely, squamous metaplasia (SM) + goblet cells (GC) (HR 46.326), foamy macrophages (FM) (HR 39.625), epithelial cells and multinucleated giant cells or cholesterin (EM) (HR 13.195), a cavernous portion of the right internal carotid artery (CP-ICA) (HR 9.427), epithelial cells with ciliated cuboidal (EC-CC) (HR 8.456), were independently associated with RCC pathological status. These divergent AUCs (0.848 for Hypo as RCC, 0.981 for RCC co PA, 0.926 for CD and CP co RCC) and subtypes of PA (HR 4.415, HR 2.286), Hypo (HR 3.310), CD and CP (HR 2.467), EC and DC and PG and SGR (HR 1.068), coexisting with the risk of a comorbid RCC lesion, may reflect the etiologic heterogeneity of coderivation and the different effects of some risk factors on tumor subtypes. Our analyses suggested that the greatest accuracy was observed for the pituitary adenoma subtype, with an AUC of 0.981 (95% confidence interval [CI]: 0.959–1.005), while the poorest accuracy was observed for aneurysms, with an AUC of 0.531 (95% CI: 0.104–0.958). We separately analyzed and confirmed the above results. Sensitivity analysis revealed no evidence of systematic bias due to missing data.ConclusionThis study showed that the histopathological changes in patients with sellar embryonic remnant-associated collision tumors showed highly consistent epithelial cell replacement (renewal) (ciliated columnar epithelium to ciliated squamous epithelium to squamous epithelium) or accumulation, and the RCC cyst wall was similar in structure to the tracheobronchial airway epithelium, with progenitor cell characteristics. The collision accuracy between RCC and other tumors (PAs, craniopharyngioma, chordoma, etc.) is different; these characteristics constitute the theoretical basis for the postmigration development of the pharyngeal bursa.